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anti-Human CFLAR Antibodies:
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Human Polyclonal CFLAR Primary Antibody for ELISA, ICC - ABIN4312113
Kim, Fisher, Xu, el-Deiry: Molecular determinants of response to TRAIL in killing of normal and cancer cells. in Clinical cancer research : an official journal of the American Association for Cancer Research 2000
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Human Monoclonal CFLAR Primary Antibody for ICC, IHC - ABIN1169018
Scaffidi, Schmitz, Krammer, Peter: The role of c-FLIP in modulation of CD95-induced apoptosis. in The Journal of biological chemistry 1999
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Human Monoclonal CFLAR Primary Antibody for IP, WB - ABIN1169019
Rescigno, Piguet, Valzasina, Lens, Zubler, French, Kindler, Tschopp, Ricciardi-Castagnoli et al.: Fas engagement induces the maturation of dendritic cells (DCs), the release of interleukin (IL)-1beta, and the production of interferon gamma in the absence of IL-12 during DC-T cell cognate ... in The Journal of experimental medicine 2000
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Human Polyclonal CFLAR Primary Antibody for WB - ABIN4312104
Garimella, Gehlhaus, Dine, Pitt, Grandin, Chakka, Nau, Caplen, Lipkowitz: Identification of novel molecular regulators of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in breast cancer cells by RNAi screening. in Breast cancer research : BCR 2014
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Human Monoclonal CFLAR Primary Antibody for FACS, IHC - ABIN1724850
Bedolla, Gong, Prihoda, Yeh, Thompson, Ghosh, Kumar: Predictive value of Sp1/Sp3/FLIP signature for prostate cancer recurrence. in PLoS ONE 2012
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Human Monoclonal CFLAR Primary Antibody for IHC, ELISA - ABIN1724856
Noh, Lee, Sung, Song, Kim, Woo, Kwon, Lee: CHOP down-regulates cFLIP(L) expression by promoting ubiquitin/proteasome-mediated cFLIP(L) degradation. in Journal of cellular biochemistry 2012
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Human Polyclonal CFLAR Primary Antibody for ICC, IF - ABIN4312114
Jones, Moskaluk, Gillenwater, Petroni, Burks, Philips, Rehm, Olazagasti, Kozower, Bao: Phase I trial of induction histone deacetylase and proteasome inhibition followed by surgery in non-small-cell lung cancer. in Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer 2012
Human Polyclonal CFLAR Primary Antibody for ICC, ELISA - ABIN1030398
Bucur, Pennarun, Stancu, Nadler, Muraru, Bertomeu, Khosravi-Far: Poor antibody validation is a challenge in biomedical research: a case study for detection of c-FLIP. in Apoptosis : an international journal on programmed cell death 2013
miRNA-708 acts as a tumor suppressor because it negatively regulates the anti-apoptotic protein c (show PROC Antibodies)-FLIPL and regulates the sensitivity of renal cancer cells to various apoptotic stimuli.
The (fli:GFP) Casper zebrafish embryo can be used as an efficient animal model to study metastatic behavior of human CM cells and warrants further testing of drug efficacy to aid care of CM patients.
Inhibition of BET bromodomain-dependent XIAP and FLIP expression sensitizes KRAS-mutated non-small cell lung cancer to pro-apoptotic agents.
the c-FLIP and NOXA (show PMAIP1 Antibodies)/Mcl-1 (show MCL1 Antibodies) axis participated in the synergistic effect of pemetrexed plus cisplatin in human choroidal melanoma cells
The strongest interaction result in relation to overall breast cancer risk was found between CFLAR-rs7558475 and current smoking (ORint = 0.77, 95% CI: 0.67-0.88, pint = 1.8 x 10(-4) ). The interaction with the strongest statistical evidence was found between 5q14-rs7707921 and alcohol consumption (ORint =1.36, 95% CI: 1.16-1.59, pint = 1.9 x 10(-5) ) in relation to ER- disease risk
findings suggest that expression of cFLIPL regulates the basal interaction of Bcl-2 (show BCL2 Antibodies) with Beclin-1 (show BECN1 Antibodies) and substantiates p53 (show TP53 Antibodies) dependent ubiquitination of Beclin-1 (show BECN1 Antibodies) during autophagic stress to determine the fate of cell death or survival.
Using the tDED filament structure as a template, structural analyses reveal the interaction surfaces between FADD (show FADD Antibodies) and caspase-8 (show CASP8 Antibodies) and the distinct mechanisms of regulation by cFLIP and MC159 through comingling and capping, respectively.
Data in this study show that cFLIPL inhibits IFN regulatory factor 3 (IRF3 (show IRF3 Antibodies)), a transcription factor central for IFN-beta (show IFNB1 Antibodies) and IFN-stimulated gene expression.
CFLAR levels were substantially decreased in the livers of subjects with NAFLD and NASH, as compared to that in nonsteatotic controls.
association of c-FLIPL and TIP49 (show RUVBL1 Antibodies) provided an additional mechanism involved in c-FLIPL-mediated functions, including Wnt (show WNT2 Antibodies) activation
c-FLIP modulation of AKT activity is crucial in controlling PERK signalling and sensitivity to endoplasmic reticulum stress.
Regulatory T cells have a high apoptosis rate ex vivo correlating with low c-FLIP expression.
In conclusion, our data indicated that miR (show MLXIP Antibodies)-150 potentially contributes to the hepatic steatosis and insulin (show INS Antibodies) resistance in NAFLD (show TSC2 Antibodies). miR (show MLXIP Antibodies)-150/CFLAR pathway may be a new therapeutic strategy against NAFLD (show TSC2 Antibodies).
Findings establish CFLAR as a key suppressor of steatohepatitis and indicate that the development of CFLAR-peptide-mimicking drugs and the screening of small-molecular inhibitors that specifically block ASK1 (show MAP3K5 Antibodies) dimerization are new and feasible approaches for NASH (show SAMSN1 Antibodies) treatment.
knockdown of cFLIPL and induced expression of FADD (show FADD Antibodies) rapidly accumulate intracellular ROS (show ROS1 Antibodies) accompanied by JNK1 (show MAPK8 Antibodies) activation to substantiate apoptosis.
CASP8 (show CASP8 Antibodies) is present exclusively as its cleaved p43 (show AIMP1 Antibodies) product, bound to cFLIPL.
The generation of mouse line with Flip deficiency in cells that express cre under the CD11c (show ITGAX Antibodies) promoter is reported.
c-FLIPL deficiency induces the caspase (show CASP3 Antibodies)-mediated processing of RTN4 (show RTN4 Antibodies), thus affecting endoplasmic reticulum (ER) shape and coupling to mitochondria. Thus, it was concluded that c-FLIPL is a novel regulator of ER morphology and ER-mitochondria crosstalk.
Acute organ failure following the loss of anti-apoptotic cellular FLICE-inhibitory protein involves activation of innate immune receptors.
The results reveal a novel inhibitory role of c-FLIP in myeloid cell activation and demonstrate the unexpected anti-inflammatory activity of c-FLIP.
results indicate downregulation of cFLIP during structural luteal regression, suggesting that cFLIP plays a survival role in the bovine corpus luteum
Conservation of FLIP's ability to inhibit apoptosis and to downregulate NF-kappaB (show NFKB1 Antibodies) activation across species.
cellular-Flice like inhibitory protein (cFLIP) long form, plays an anti-apoptotic role in the granulosa cells of healthy follicles of pig ovaries [cFLIP]
Intracellular remodeling with overexpression of pig c (show PIGC Antibodies)-FLIP in xenograft cells may decrease the innate cellular responses against xenografts, facilitating long-term xenograft survival.
Intracellular remodeling with the overexpression of c-FLIP(S/L) in xenograft cells may avoid innate cellular attacks against xenografts and facilitate long-term xenograft survival.
Overexpression of c-FLIP in xenograft cells may prevent innate cellular attacks against xenografts opening the window of opportunity for long-term xenograft survival.
The protein encoded by this gene is a regulator of apoptosis and is structurally similar to caspase-8. However, the encoded protein lacks caspase activity and appears to be itself cleaved into two peptides by caspase-8. Several transcript variants encoding different isoforms have been found for this gene, and partial evidence for several more variants exists.
, CASP8 and FADD-like apoptosis regulator
, flice/caspase-i inhibitory protein
, cellular FLICE-like inhibitory protein
, CASP8 and FADD-like apoptosis regulator-like
, FADD-like anti-apoptotic molecule
, FADD-like antiapoptotic molecule 1
, MACH-related inducer of toxicity
, caspase homolog
, caspase-eight-related protein
, caspase-like apoptosis regulatory protein
, caspase-related inducer of apoptosis
, inhibitor of FLICE
, usurpin beta
, FLICE-like inhibitory protein